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Biomedical subjects

K Nomiyama

Publications and source records attributed to K Nomiyama.

At least 73 records · Page 4Linked to original sources
PubMed1986

[Negative report on trichloroethylene-induced pneumatosis cystoides intestinalis in rats].

In recent years it has been suggested in Japan that occupational trichloroethylene exposure will induce primary pneumatosis cystoides intestinalis coli. A series of two experiments were conducted to ascertain the cause-effect relationship between trichloroethylene and pneumatosis as follows: In the first experiment, 12 male rats of Fischer strain were exposed to trichloroethylene at a nearly lethal concentration for 12 wk. Five out of 12 rats died during the experiment, and body weight gain was extremely depressed. However, neither pneumatosis nor histological changes were observed. No changes were observed in 4 control rats as well. In the second experiment, 38 male rats of Sprague-Dawley strain were exposed to 800, 200 or 50 ppm trichloroethylene over a period of 12 wk. Two out of 13 rats of the 800 ppm group died, and body weight gain was suppressed. Mild suppression in body weight gain was also observed in the 200 ppm group. However, pneumatosis was not observed in any rats of trichloroethylene groups. No pathological changes were observed in 13 rats of the control group. The foregoing results suggest that trichloroethylene cannot induce pneumatosis cystoides intestinalis in rats of these two strains. Inasmuch as rats are not prone to develop pneumatosis, the possibility for trichloroethylene to induce this disease in man cannot be denied.

Animals↗
PubMed1984

Reversibility of cadmium-induced health effects in rabbits.

Twenty-one male rabbits were divided into three groups: rabbits of two groups were given pelleted food containing cadmium chloride at a dose level of 300 micrograms Cd/g over periods of 44 or 19 weeks. Rabbits of the last group were given ordinary commercial pelleted food and served as controls. Cadmium increased urinary protein and amino acid by week 19 and increased it to a remarkably high level by week 44. After cessation of cadmium exposure, rabbits of the first group (44 weeks exposure group) showed only little recovery from cadmium health effects: proteinuria and aminoaciduria were slightly improved. Depressed hepatic functions were also slightly improved, but did not return to the control level in 24 weeks. Fat and bone metabolism also remained depressed below the control level. Anemia did not also readily recover. On the other hand, rabbits of the second group (19 weeks exposure) recovered from the effects of cadmium: proteinuria and aminoaciduria in most animals disappeared soon after the end of cadmium exposure, plasma GPT fell after 1 week, and hemoglobin and hematocrit returned to normal in 6-11 weeks. The above results show that after cessation of cadmium exposure, mild cadmium-induced health effects were reversible in a short period, while more severe effects were not readily reversible. High performance liquid chromatographic (HPLC) profiles of renal and hepatic cadmium-thionein (Cd-MT) during and after exposure to cadmium showed no correlation to the degree of cadmium health effects, and therefore, did not help to elucidate mechanisms of the recovery from cadmium-induced health effects, probably because cadmium not bound with metallothionein (non-MT-Cd) is responsible for inducing renal effects.

Amino Acids↗
PubMed1983

[Mechanism of beta 2-microglobulinuria in experimental chronic cadmium intoxication].

Natural history of cadmium health effects was studied on monkeys and rabbits given cadmium chloride orally or subcutaneously for a long period: 6 male monkeys were given pelleted food containing 100 micrograms Cd/g over a period of 180 weeks, 15 male rabbits pelleted food containing 300 micrograms Cd/g over a period of 24 weeks, 13 male rabbits daily subcutaneous injections at a dose level of 0.5 mg Cd/kg over a period of 44 weeks, and 23 rabbits subcutaneous injections at a dose level of 0.5 mg Cd/kg 6 times a week over a period of 21 weeks, respectively. Sodium dodecyl polyacrylamide gel electrophoresis and silver staining (detection limit of protein: 80 micrograms/dl) revealed that urinary protein of molecular weight 12,000 (probably beta 2-microglobulin) increased slightly prior to the appearance of proteinuria, glycosuria or aminoaciduria. Remarkable increase in urinary protein of molecular weight 12,000 was observed by Amidoblack 10 B staining (detection limit: 4 mg/dl) around the time when renal dysfunctions appeared. The above result might suggest that the remarkable increase in urinary beta 2-microglobulin is associated with renal dysfunctions, while the slight increase is caused by other mechanisms than renal dysfunctions.

Administration, Oral↗
PubMed1982

[Carcinogenicity of cadmium].

Cadmium has been thought to be carcinogenic for these ten years. The present author reviewed 98 papers on its carcinogenicity. Ten papers describing epidemiological studies on cadmium workers, re-evaluated by the present author, do not derive a solid conclusion that cadmium is carcinogenic. However, there still exists a certain probability that cadmium is a weak carcinogenic substance in the human, because of some data on chromosomal aberrations in cadmium workers, tumorigenesis at the site of cadmium injection in animals, and Leydig cell tumor formation in animals given subcutaneous injections of cadmium.

Animals↗
PubMed1981

Retinol-binding protein and beta 2-microglobulin in urine of cadmium-fed rhesus monkeys.

Retinol-binding protein (RBP) in the Rhesus monkey had the same electrophoretic mobility, molecular weight, and common antigens as human RBP; beta 2-microglobulin protein (MG) had similar electrophoretic mobility and partial common antigens to human MG. After a prolonged oral administration of cadmium chloride to 10 monkeys over a period of 55 weeks, one monkey of the 30 mg Cd/day group indicated RBPuria and MGuria with the use of anti-human RBP and MG sera when proteinuria appeared. The immunological assay of low-molecular-weight proteins in urine was not applicable for the early detection of cadmium health effects in monkeys.

Animals↗